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Evaluation of apoptotic pathways in dorsal root ganglion neurons following peripheral nerve injury.

Authors: Wiberg, Rebecca  Novikova, Liudmila N  Kingham, Paul J 
Citation: Wiberg R, etal., Neuroreport. 2018 Jun 13;29(9):779-785. doi: 10.1097/WNR.0000000000001031.
Pubmed: (View Article at PubMed) PMID:29659443
DOI: Full-text: DOI:10.1097/WNR.0000000000001031

Peripheral nerve injuries induce significant sensory neuronal cell death in the dorsal root ganglia (DRG); however, the role of specific apoptotic pathways is still unclear. In this study, we performed peripheral nerve transection on adult rats, after which the corresponding DRGs were harvested at 7, 14, and 28 days after injury for subsequent molecular analyses with quantitative reverse transcription-PCR, western blotting, and immunohistochemistry. Nerve injury led to increased levels of caspase-3 mRNA and active caspase-3 protein in the DRG. Increased expression of caspase-8, caspase-12, caspase-7, and calpain suggested that both the extrinsic and the endoplasmic reticulum (ER) stress-mediated apoptotic pathways were activated. Phosphorylation of protein kinase R-like ER kinase further implied the involvement of ER-stress in the DRG. Phosphorylated protein kinase R-like ER kinase was most commonly associated with isolectin B4 (IB4)-positive neurons in the DRG and this may provide an explanation for the increased susceptibility of these neurons to die following nerve injury, likely in part because of an activation of the ER-stress response.


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RGD Object Information
RGD ID: 13782273
Created: 2018-08-31
Species: All species
Last Modified: 2018-08-31
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.